The current proposal seeks to define the impact of FSHR phosphorylation on the functions of FSHR, and to further understand the mechanisms involved in phosphorylation. Specifically, it is proposed to: 1) use site-directed mutagenesis to identify the amino acid residues which are phosphorylated in response to FSH and PMA and to examine the functional consequences of FSH- and PMA-induced FSHR phosphorylation; and 2) identify the protein kinases that phosphorylate the FSHR. By analogy with the beta adrenergic receptor, it is reasonable to propose that phosphorylation of the FSHR may be involved in the termination of the actions of FSH and in the regulation of the functions of FSHR by other hormones. In the face of constant hormone levels, a lack of regulation at the level of the receptor would result in hyperstimulation of the target cells.